Correspondence Address: Prof. Vaishal S Shah 10-D, Raj Bhawan Road, Opposite SBBJ, Civil Lines, Kota – 324001, Rajasthan. India
Source of Support: None, Conflict of Interest: None
Hypoglycemia is associated with adrenergic and various neurological symptoms including hemiparesis. Though not common, movement disorders such as chorea and ballism have been reported in hypoglycemia. This case was of an elderly lady, a known diabetic, who developed two episodes of hemiparesis and single episode of jerky head movement with preserved sensorium lasting for few seconds, associated with hypoglycemia on different occasions, 1 week after increasing the dosage of oral hypoglycemic agent with complete recovery each time with correction of sugar levels. Magnetic resonance imaging showed transient bilateral diffusion restriction in posterior limb of internal capsule.
Keywords: Hemiparesis, hypoglycemia, jerky head movement
How to cite this article: Shah VS, Sardana V. Sudden jerky head movement in hypoglycemia. Ann Mov Disord 2020;3:44-6
Hypoglycemia has been associated with various abrupt neurological symptoms including confusion, coma, and seizure. Presentation as a hemiparesis is also observed in approximately 4.2% of cases., Few reports of dyskinetic movements including chorea and hemiballismus have been also reported., To the best of our knowledge, jerky head movement is not reported till now in hypoglycemia.
A 64-year-old female patient reported to our hospital with a history of type 2 diabetes mellitus for last 10 years on metformin 1000mg. One week before admission, glimepiride 4mg was added for glycated hemoglobin of 7.2 %. Four days after drug modification, she developed left hemiparesis without autonomic symptoms, which recovered in 5min after administering lemon water with sugar at home as a part of traditional practice. She was continuing oral hypoglycemic agents. Again, similar episode occurred after 2 days, from which she did not recover. Hence, the patient was brought to the hospital. Her blood pressure was 130/70mm Hg. Her sensorium was normal with a power of 3/5 on left side at admission. Capillary blood glucose level was 44mg/dL, which improved with 25% dextrose along with complete recovery of hemiparesis. Computed tomography of brain was normal. Rest of the blood investigations, including renal and liver function tests, was normal.
On the evening of the admission day, she developed involuntary jerky to and fro head movement lasting for around 30s, later involving right upper limb as well with preserved sensorium [Video 1]. Blood sugar level was 30mg/dL at the end of this episode, which improved with dextrose infusion. For the next 24h, she was on maintenance 5% dextrose without further episode of hypoglycemia. Magnetic resonance imaging (MRI) of brain performed on the next day showed diffusion restriction in posterior limb of internal capsule bilaterally with normal T2 and fluid-attenuated inversion recovery (FLAIR) images consistent with hypoglycaemia [Figure 1]. Electroencephalogram showed diffuse theta and delta slowing without focal/generalized discharges. There was no recurrence of similar movements during hospital stay. She was discharged with drug modification. Repeat MRI after 2 months was found to be normal.
Figure 1: (A) Normal apparent diffusion coefficient image at disease onset. (B) Diffusion restriction in bilateral posterior limb of internal capsule at disease onset. (C) Normal apparent diffusion coefficient image after 2 months. (D) Resolution of restricted diffusion
Lawrence Tierney stated: “A stroke is never a stroke until it has received 50 of D50.” This maxim highlights hypoglycemic hemiparesis and means that hypoglycemia should not be forgotten when treating a patient who is suspected to have had a stroke.
Our case developed recurrent hypoglycemia leading to two episodes of left hemiparesis and one episode of jerky head movement probably due to glimepiride, which was added 4 days before the first episode of hemiparesis. Absence of autonomic symptoms in our patient probably suggests hypoglycemic unawareness due to recurrent hypoglycemic episodes. Similarly, a study conducted by Malouf and Brust also noted the absence of adrenergic symptoms in 125 patients who presented with neurological manifestation.
Structures commonly involved in hypoglycemia are posterior limb of internal capsule, cortex, corona radiata, hippocampus, and basal ganglia., Predilection for these structures is because of regional variability in glucose level, arrest of protein synthesis and neuronal necrosis, and difference in amino acid distribution. Our case had the involvement of bilateral posterior limb of internal capsule in the form of diffusion restriction. Diffusion restriction in hypoglycemia occurs because of excitotoxic edema, which results from increased extracellular glutamate, which is reversible if corrected early as observed in our case.
Hemiparesis is a known but uncommon presentation of hypoglycemia. Similar to our case, reversible radiological involvement of bilateral internal capsule is frequently observed in case of hypoglycemic hemiparesis. The pathogenesis behind unilateral clinical presentation with bilateral radiological involvement is not well understood. Possible hypothesis is asymmetric blood flow and selective neuronal vulnerability. Most of the time, recovery of hemiparesis occurs in 15min, once normoglycemia is achieved, but few cases in the past have taken 3 days as well.
Movement disorders such as chorea and ballism have been reported in hypoglycemia but the exact pathogenesis is not well understood., The aspartate, an excitatory neurotoxin released in hypoglycemia in cerebral cortex, corpus striatum, and hippocampus, induces involuntary movements. Single photon emission computed tomography imaging in patients with hypoglycemia and chorea has shown decreased blood flow in the basal ganglia and increased perfusion of the thalamus contralateral to the side of the body manifesting chorea. These findings have led to speculation that decreased pallidal inhibitory input to the thalamus, resulting in increased thalamocortical outflow, might explain hyperkinesia. MRI in these cases revealed changes in corpus striatum, whereas in our case, posterior limb of internal capsule was involved., Therefore, it is possible that jerky head movement can be different from the movement disorders commonly observed in hypoglycemia. Similar to this case, a study conducted by Nakajima et al. also reported a case of jerky leg movement in hypoglycemia with similar imaging findings. Loss of connection between corticospinal pathway and lower motor neuron in hypoglycemia, leading to disorganized fragments of polysegmental spinal reflex, causing abnormal jerky movement, might be the possible explanation of movement disorder due to the involvement of posterior limb of internal capsule. Second possibility could be the involvement of close by structure involving pallidothalamic fibers.
Existence of cases in which hypoglycemia cannot be distinguished from stroke on imaging studies suggests the importance of measurement of blood glucose level when stroke symptoms are first recognized. Our case also highlights the occurrence of jerky head movement in hypoglycemia, which is not among the list of common movement disorders associated with hypoglycemia.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Gorell JM, Dolkart PH, Ferrendelli JA. Regional levels of glucose, amino acids, high energy phosphates, and cyclic nucleotides in the central nervous system during hypoglycemic stupor and behavioral recovery. J Neurochem 1976;27:1043-9.
Kim JS, Lee KS, Lee KH, Kim YI, Kim BS, Chung YA, et al. Evidence of thalamic disinhibition in patients with hemichorea: Semiquantitative analysis using SPECT. J Neurol Neurosurg Psychiatry 2002;72:329-33.